Optimisation of preparation conditions for Ti nanowires and suitability as an antibacterial material

Ultrafine titanium dioxide (TiO₂) nanowires were synthesised using a hydrothermal method with different volumes of ethylene glycol (EG) and annealing temperatures. It shows that sodium titanate nanowires synthesised using 5 and 10 ml EG, which annealed at 400°C produced TiO₂ nanowires that correspond to a photochemically active phase, which is anatase. The influences of annealing temperatures (400–600°C) on the morphological arrangement of TiO₂ nanowires were evident in the field emission scanning electron microscopy. The annealing temperature of 500°C led to agglomeration, which formed a mixture of TiO₂ nanoparticles and nanowires. High thermal stability of TiO₂ nanowires revealed by thermogravimetric analysis and Fourier transform infrared spectroscopy spectrum showed the presence of the Ti–O–Ti vibrations as evidenced due to TiO₂ lattices. An antibacterial study using TiO₂ nanowires toward Escherichia coli and Klebsiella pneumoniae showed large zones of inhibition that indicated susceptibility of the microbe toward TiO₂. Growth kinetic analysis shows that addition of TiO₂ has reduced optical density (OD) suggesting an inhibition of the growth of bacteria. These results indicate TiO₂ nanowires can be effectively used as an antimicrobial agent against gram‐bacteria. The TiO₂ nanowires could be exploited in the medical, packaging and detergent formulation industries and wastewater treatment.Inspec keywords: nanowires, titanium compounds, antibacterial activity, nanomedicine, semiconductor materials, semiconductor growth, nanofabrication, annealing, liquid phase deposition, field emission scanning electron microscopy, nanoparticles, thermal stability, thermal analysis, Fourier transform infrared spectra, microorganismsOther keywords: optimisation, preparation conditions, antibacterial material, ultrafine titanium dioxide nanowires, hydrothermal method, ethylene glycol, annealing temperatures, sodium titanate nanowires, photochemically active phase, anatase, morphological arrangement, field emission scanning electron microscopy, agglomeration, nanoparticles, thermal stability, thermogravimetric analysis, Fourier transform infrared spectroscopy, vibrations, Escherichia coli, Klebsiella pneumoniae, microbe, growth kinetic analysis, optical density, incubation time, bacterial survivability, colony‐forming units, antimicrobial agent, Gram negative bacteria, Gram positive bacteria, temperature 400 degC to 600 degC, TiO₂      

Inflammatory and Proliferative Pathway Activation in Human Esophageal Myofibroblasts Treated with Acidic Bile Salts

Subepithelial human esophageal myofibroblasts (HEMFs) in gastroesophageal reflux disease (GERD) are exposed to luminal contents via impaired squamous epithelium barrier integrity. The supernatant of HEMFs treated with acidic bile salts reflective of in vivo reflux increases squamous epithelial thickness. We aimed to identify the involved mechanisms using an unbiased approach. Acidic-bile-salt-treated primary HEMF cultures (n = 4) were submitted for RNA-Seq and analyzed with Partek Flow followed by Ingenuity Pathway Analysis (IPA). A total of 1165 molecules (579 downregulated, 586 upregulated) were differentially expressed, with most top regulated molecules either extracellular or in the plasma membrane. Increases in HEMF CXCL-8, IL-6, AREG, and EREG mRNA, and protein secretion were confirmed. Top identified canonical pathways were agranulocyte and granulocyte adhesion and diapedesis, PI3K/AKT signaling, CCR5 signaling in macrophages, and the STAT3 pathway. Top diseases and biological functions were cellular growth and development, hematopoiesis, immune cell trafficking, and cell-mediated response. The targets of the top upstream regulator ErbB2 included CXCL-8, IL-6, and AREG and the inhibition of CXCL-8 in the HEMF supernatant decreased squamous epithelial proliferation. Our work shows an inflammatory/immune cell and proliferative pathways activation in HEMFs in the GERD environment and identifies CXCL-8 as a HEMF-derived chemokine with paracrine proliferative effects on squamous epithelium.